The editorial board of the International Journal of Cardiology regretfully report a paper we are formally retracting from the scientific literature due to an unexplained and unacceptable textual similarity with previously published work with neither attribution nor permission. It was reported to me by Dr. Hawkin Woo that the paper by Abu-Hilal published in the International Journal of Cardiology bore a striking resemblance to his earlier work published in his 2006 article in History of Medicine Online . The manuscript published by Dr. Hawkin Woo stands and there is no criticism of the authors of this paper.

The text which is identical between the two papers is copied below:

“He soon fell into the fold of the “Oxford Experimental Philosophical Clubbe” whose “virtuosi” included Robert Boyle (1627-1691), Thomas Willis (1621-1675), and John Locke (1631-1691). (Dewhurst, 1980) Lower had a gift as an anatomical dissector which caught the attention of Willis, who put him and Christopher Wren (1632-1723) to work in the anatomy lab. Their efforts produced a masterpiece, Cerebri anatome. (Willis, 1664/1971) In the treatise’s introduction, Willis celebrated Lower as “a most Learned Physician and highly skilful Anatomist.”

“In De Corde Lower also demonstrated a keen understanding of the pericardium. He recognized the consequences of excessive fluid accumulation in the pericardial space, i.e. pericardial effusion: “The fluid enclosed in the pericardium renders great service in lubricating the surface of the heart and in facilitating its movement; it likewise occasionally oppresses and floods the heart when it is in excess.”

“Lower astutely recognized the converse, i.e. the consequences of pericardial fluid absence. He hypothesized a constrictive situation for the heart: For, just as it [pericardium] injures the heart by accumulation of fluid within in, so, when this is completely absent, it approaches so close to the heart, that at length it adheres everywhere to this organ….How great a hindrance and disadvantage this must be for both organs….”

“Lower went on to illustrate a case of constrictive pericarditis. In describing the case, he makes a discerning observation on the pulse that would foreshadow Kussmaul, i.e., the paradoxical pulse: ““The wife of a certain citizen of London, aged 30, healthy and active enough previously, became very dejected and melancholy during the last three years of her life, suffered from breathlessness on the least exertion, had a small and often an intermittent pulse.”

“Adolf Kussmaul (1822-1902) is a well recognized figure in the history of medicine. Eponyms like Kussmaul’s sign and Kussmaul breathing give him instant recognition to clinicians”

“Kussmaul started his medical career as a country doctor. However, his career was cut short due to a severe illness, self-diagnosed as “meningitis”. (Kussmaul, 1899/1981) Upon recovery, he “renounced the country practice” feeling he “was no longer equal to it” and turned to a career in academic medicine in 1853. (Kussmaul, 1899/1981) He meticulously prepared for an academic career with coursework at Wurzburg (Kussmaul, 1899/1981). He spent about a year building up his credentials learning from the likes of Rudolph Virchow.”
“Kussmaul originated the term pulsus paradoxus in 1873 with the publication of Ueber schwielge mediastinopericarditis und den paradoxen puls (On adhesive mediastino-pericarditis and the paradoxical pulse). (Kussmaul, 1873/2006) In the document Kussmaul carefully described three cases of constrictive pericarditis and pulsus paradoxus with meticulous clinical observation. In each case, he draws attention to “an interesting phenomenon” of the pulse, exemplified in the excerpt: “A 34 year old unemployed servant girl, whose mother had died of pulmonary disease, had suffered for many years each winter from a dry cough and for three years a constricting feeling which at times became dyspnea….On admission, she appeared cachectic, with edema of the legs and ascites. The phenomenon of the arterial pulse with regular and constant action of the heart was observed at the initial examination. The pulse would become smaller with inspiration or would become totally impalpable on deep inspiration. On expiration it returned to its former amplitude…. The disappearance or diminution of the pulse during inspiration was manifest in all palpable arteries.”

“Kussmaul hypothesized about the pathophysiology of pulsus paradoxus in constrictive pericarditis. He came to a similar conclusion as Lower that somehow the physical adherence of the pericardium to a nearby structure was critical: “The essential anatomic condition for the development of the paradoxical pulse appears to be the adherence between the pericardium and the sternum…””

“Kussmaul noted that pulsus paradoxus was not unique to constrictive pericarditis, describing the phenomenon in a patient with a massively dilated right main bronchus from tuberculosis. He concluded that: “...the paradoxical pulse may also occur without pericarditis. This sign is consistently a result of mediastinal disease, and we may only assume that it is mediastino-pericarditis when the history, onset, and course of the disease present as additional criteria for the diagnosis of pericarditis.” ”

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